RalA and RalB are Ras-family small monomeric GTPases that can be activated through a Ras-dependent mechanism. The two are highly homologous (89%). RalA is required for anchorage-independent proliferation and tumorigeneisis by driving exocyst assembly and polarizatied exocystossis in epithelaial cells (Cascone, 2008). RalB is required for metastatic formation and cell survival by driving exocyst assembly during polarized cell migration (Cascone, 2008). Ral proteins are proximal effectors of oncogenic Ras and their activity is needed to support tumorigenesis in certain cancers. Mutants of Ras that are defective in activating all known Ras effectors except Ral GEF are still able to induce invasive phenotypes in transfected cells, suggesting a role for Ral in these processes